中文摘要：

目的：探讨右美托咪定对大鼠肢体缺血-再灌注后急性肺损伤的影响及机制。方法：将60只清洁健康级雄性Wistar大鼠随机分为4组：对照组、缺血再灌注组、预处理组和后处理组，每组15只。光镜下观察每组肺组织病理学改变并计算中性粒细胞。测定肺组织湿干比（W／D）和动脉血PaO2、肺组织细胞因子肿瘤坏死因子（TNF-α）、白介素IL-6和IL-10的含量及肺组织脂质氧化产物丙-~（MDA）含量。结果：大鼠肢体缺血一再灌注后可引起肺组织出现损伤性变化。与缺血再灌注组比较，预处理组和后处理组大鼠肺组织的病理改变明显减轻；与对照组比较，缺血再灌注组、预处理组和后处理组的TNF-（3L、IL-6、IL-10和MDA明显升高．其中预处理组和后处理组的TNF-α、IL-6和MDA明显低于缺血再灌注组．而预处理组和后处理组的IL-10明显高于缺血再灌注组。结论：非特异性炎性反应和氧化应激介导了大鼠肢体缺血一再灌注所致的急性肺损伤．右美托咪定可以抑制上述介导机制。从而减轻大鼠肢体缺血一再灌注所致的急性肺损伤。

英文摘要：

Objective To investigate the effects of dexmedetomidine on acute lung injury induced by hind limb ischemia-reperfusion in rats. Methods Sixty healthy male Wistar rats were randomly allocated into 4 groups ： group C （control）, group I-R （ischemia-reperfusion）, group Pre-Dex （dexmedetomidine） and group Post- Dex. The morphological changes of the lung tissues were observed under light microscope, and polymorphonuelear neutrophils （PMN） in alveolar septum were counted. Meanwhile, lung coefficient, arterial partial PaO2, lung levels of tumor necrosis factor （TNF）-ct, interleukin （IL）-6, interleukin （IL）-10, and malondialdehyde （MDA） were measured. Results Rats in the I-R group were resulted in the damage of the lung tissues. The rats in group Pre-Dex and group Post-Dex were featured with obvious mild lung injury. TNF-cL,IL-6,IL-10 and MDA in lung levels were significantly increased in group I-R, Pre-Dex and Post-Dex. TNF-c~, IL-6 and MDA in the lung were significantly decreased in group Pre-Pex and group Post-Dex. IL-10 was increased in group Pre-Dex and group Post-Dex. Conclusions Inflammatory response and oxidative stress are involved in the pathogenesis of acute lung injury induced by hind limb ischemia-reperfusion in rats. Dexmedetomidine attenuated the lung injury through anti-inflammation and anti-oxidation.